Syringin Exerts Anti-Breast Cancer Effects Through PI3K-AKT and EGFR-RAS-RAF Pathways

Abstract

Background Breast cancer (BC) is one of the most common malignant tumors with the highest mortality in the world. Modern pharmacological studies have shown that Syringin has an inhibitory effect on many tumors, but its anti-BC efficacy and mechanism are still unclear. Methods First, Syringin was isolated from Acanthopanax senticosus (Rupr. & Maxim.) Harms (AS) by systematic solvent extraction and silica gel chromatography column. Then, the potential mechanism of syringin against BC was revealed by bioinformatics and in vitro experiments. To provide a more experimental basis for later research, the hub genes which could be candidate biomarkers of BC and a ceRNA network related to them were obtained. Results Syringin was obtained by liquid chromatography-mass spectrometry (LC-MS), nuclear magnetic resonance (NMR), and high-performance liquid chromatography (HPLC). Bioinformatics results showed that MAP2K1, PIK3CA, HRAS, EGFR, Caspase3, and PTGS2 were the hub targets of Syringin against BC. In vitro experiments confirmed that Syringin inhibited the proliferation and migration and promoted apoptosis of BC cells through the above hub targets. And PIK3CA and HRAS were related to the survival and prognosis of BC patients, the PIK3CA-has-mir-139-5p-LINC01278 and PIK3CA-has -mir-375 pathways might be closely related to the mechanism of Syringin against BC. Conclusions Syringin against BC via PI3K-AKT-PTGS2 and EGFR-RAS-RAF-MEK-ERK pathways, and PIK3CA and HRAS are hub genes for adjuvant treatment of BC.